What impact does maternal obesity have on fetal growth?

Results of a study of fetal ultrasounds show that maternal obesity has an impact on fetal growth as early as 32 weeks’ gestation. However, the mechanisms behind the association and the implications of the findings, published in JAMA Pediatrics, remain to be determined.

For the longitudinal study, researchers looked at cohort of 443 obese (prepregnancy body mass index [BMI] >30) and 2,320 nonobese pregnant women (prepregnancy BMI 19 to 29.9) at 12 US health care institutions. None of the women had major chronic diseases and their pregnancies all were from 8 weeks, 0 days’ to 13 weeks, 6 days’ gestation.  The participants were randomized to 1 of 4 schedules of 2- and 3-dimensional ultrasonograms to capture weekly fetal growth for the remainder of their pregnancies.

The authors measured fetal humerus length, femur length, biparietal diameter, head circumference, and abdominal circumference on each ultrasonogram and estimated fetal growth curves using linea mixed models with cubic splines. Likelihood ratios and Wald tests after adjustment for maternal characteristics were used to look at median differences in fetal measures at each gestational week in obese versus nonobese women.

Fetuses of obese women had significantly longer femurs and humeruses than those of nonobese women, beginning at 21 weeks’ gestation. The differences persisted through 38 weeks’ gestation (median femur length 71.0 vs 70.2 mm; P = .01; median humerus length 62.2 vs 61.6 mm; P = .03). Averaged across gestation, head circumference was significantly larger in fetuses of the obese women versus those in nonobese women (P = .02) Fetuses of the obese women were significantly larger than those of women of normal weight beginning at 32 weeks (median 282.1 vs 280.2 mm; P = .04) Estimated fetal weight was also significantly higher in fetuses of obese women, starting at 30 weeks’ gestation (median 1512 g [95% CI, 1494-1530 g] vs 1492 g [95% CI, 1484-1499g] and it increased with gestational age. In neonates born to obese women, birth weight was higher by almost 100 g than in neonates born to the nonobese women (mean 3373.2 vs 3279.5 g).

NEXT - Study: Consuming processed meats can increase risk of breast cancer

Study: Consuming processed meats can increase risk of breast cancer

Breast cancer risks increased by 21% in women who consumed more than 9 g of processed meat per day, according to a study published in The European Journal of Cancer. The study looked at the consumption of both processed meat and red meat but found that red meat was not associated with breast cancer.

The researchers used data from the UK Biobank, an ongoing general population cohort study, which recruited participants aged 40 to 69 (n = 500 000 adults). Breast cancer incidence was determined through cross-referencing routine hospital admission, cancer registry, and death certificate data. Once the study population had been set, the researchers used univariate data and multivariable Cox proportional hazard models to explore any link between red meat, processed meat (red meat that has been salted, cured, fermented, smoked or undergone other processes), and breast cancer. Additionally, the researchers performed a meta-analysis using a random effects model of published cohort studies to expand the study.

The study identified 262,195 women aged 40 to 69s from the UK Biobank study. Of them women, 4,819 women (1.84%) were diagnosed with breast cancer over a median of 7 years of follow-up. Risk of breast cancer was increased in the highest tertile (> 9 g/day) of processed meat consumption (adjusted hazard ratio [HR] 1.21, 95% confidence interval [CI] 1.08-1.35, P = 0.001). After accounting for other dietary factors, as well as sociodemographic factors and weight, the findings from the UK Biobank data still remained significant. Collation with 10 previous cohort studies returned data on 40,257 (2.44%) incident breast cancers out of 1.65 million women. Once again, processed meat consumption was associated with overall (relative risk [RR] 1.06, 95% CI 1.01-1.11) and postmenopausal (RR 1.09, 95% CI 1.03-1.15), but not premenopausal (RR 0.99, 95% CI 0.88-1.10) breast cancer. Red meat consumption was not associated with breast cancer in either the UK Biobank or the meta-analysis (adjusted HR 0.99, 95% CI 0.88-1.12 and RR 1.03, 95% CI 0.99-1.08, respectively).

The authors noted some limitations of the study. The data from the UK Biobank study were not a representative sample of the UK population since women participating in the study were generally wealthier and healthier. The data are also reliant on the participants accurately reporting how much processed meat they ate. In addition, while the UK Biobank study data accounted for dietary factors, not all of the studies included in the meta-analysis did. Ultimately, the authors suggest that more research is needed, but the findings were significant enough that physicians should educate their patients, especially women who are postmenopausal, about the correlation between intake of processed meat and breast cancer risk.

NEXT: Does prenatal use of topiramate increase risk of cleft palate?

Does prenatal use of topiramate increase risk of cleft palate?

First-trimester use of the anti-seizure medication topiramate may be associated with an increased risk of cleft palate in offspring, according to the authors of a new population-based cohort study. Published in Neurology, the findings suggest that the relationship is more pronounced the higher the dose of the drug a woman receives.

More than 1.3 million women with live-born infants were included in the research, which was based on Medicaid data from 2000 to 2010. All of the women had been enrolled in Medicaid from 3 months before conception until 1 month after delivery. The oral clefts were reported in claims during the first 3 months of the infants’ lives.

For the study, the authors compared outcomes in infants of women who were dispensed topiramate during the first trimester and in those who were not dispensed the drug and an active reference group of women who received lamotrigine during the first trimester. Generalized linear models were used to estimate risk ratios with fine stratification on the propensity score of treatment to control for potential confounders. Stratified analyses by indication and dose also were performed.

In the 2,425 infants born to women exposed to topiramate, risk of oral cleft at birth was 4.1 per 1,000 versus 1.1 per 1,000 in infants born to the unexposed women (RR 2.90, 95% confidence interval [CI] 1.56-5.40). The RR was 8.30 (95% CI 2.65-26.07) in women with epilepsy whereas it was 1.45 (95% CI 0.54-3.86) in those who took topiramate for other indications such as bipolar disorder. Women with epilepsy took a median daily dose of 200 mg of topiramate during the first trimester versus 100 mg for women without epilepsy. The RR for oral clefts was 5.16 for doses > 100 mg versus 1.64 for doses ≤ 100 mg.